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Human Physiology – Muscle

Action potentials in nerve and muscle

In muscle

- Entire muscle neurone is involved
...

- Velocity over skeletal muscle fibre is 18 times slower then nerve
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- Nerve conduction velocity is 18 times faster than muscle
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Remember an effecter does the effect
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Electrical
- Ionic current spreads to the next cell through gap junctions
- It’s a 2 way transmitter, its faster and capable of synchronising groups of neurones
...
chemical
- one way info transfer from a pre synaptic neurone to a post synaptic neurone
...

Action potential reaches the end bulb and
voltage gates ca2+ channels open – remember voltage
channels open from a change in membrane potential
2
...

3
...

This activates the post synaptic area
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The synaptic delay is 0
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– attached to the sacs in the pre synaptic
area and it takes the neurotransmitter back up













EPSP and IPSP

EPSP – Excitatory postsynaptic potential

- Graded depolarisation that moves the membrane potential closer to the threshold
for firing an action potential ( which you should know by now is -70mV)

IPSP – Inhibitory post synaptic potential

- Graded hyperpolarisation that moves the membrane potential further from the
threshold potential for firing an action potential
...
–
remember a neurone receives many of these
...
But remember homeostasis means we
have to balance everything
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Possible drug effects on Synaptic effectiveness

1- Release and degradation of neurotransmitter inside the cell or reduced degradation of
the neurotransmitter (never reaches the post synaptic cleft)
2- Increased neurotransmitter release (to aid weak transmission between the 2 synaptic
bulbs)
3- Prevention of neurotransmitter release into synapse or inhibition of synthesis of the
neurotransmitter (for patients who have too many of these happening)
4- Reduced reuptake of the neurotransmitter (for those who take up too much)
5- Agonists and antagonists (bind and revoke same response as neurotransmitter or bind
to block it from binding
...
(to stop the signal going in the first
place)




Tubocurarine: Cholinergic antagonist – we covered antagonists above
- Competitive antagonist of nicotinic neuromuscular acetylcholine receptors
- Used to paralyse patients undergoing anaesthesia

NMJ – Neuromuscular junction

- End of fibre the axon nears the muscle as its motor end plate region (they remain
separated by synaptic cleft or gap)
- Botulinum toxin (remember dr walshes lectures!) blocks release of neurotransmitter
at the NMJ so muscle contraction can not occur – bacteria found in improperly
canned food = death occurs from paralysis of the diaphragm
- Curare (plant poison from poison arrows) – causes muscle paralysis by blocking the
ACh receptors – used to relax muscle during surgery
- Neostigmine (anticholinesterase agent) – blocks removal of ACh from receptors so
strengthens weak muscle contractions of myasthenia gravis – also an antidote for
curare after surgery is finished


Muscle tissue

- Alternating contractions and relaxation of cells
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3 types of muscle:

1
...

- Voluntary control of contraction and relaxation
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Cardiac muscle
- Striated in appearance
- Involuntary control
- Auto rhythmic because of built in pacemaker

3
...

- The fibres caution T tubules and sarcoplasm
- T tubules are tiny invagination of the sarcolemma that quickly spread the muscle
action potential to all parts of the muscle fibre
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Transverse Tubules

- T (transverse) tubules = invagination of the sarcolemma into the centre of the cell
- these are filled with extra cellar fluid
- carry muscle action potentials down into cell
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Sarcoplasmic reticulum

- system of tubular sacs similar to smooth ER in non muscle cells
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The thick and filaments overlap

- Proteins of the muscle :
- Myofibrils are built of 2 kinds of protein
- Contractile proteins: myosin and actin
- Regulatory proteins which turn contraction on and off : troponin and tropomyosin
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- Myosin heads (cross bridges) extend towards the thin filaments
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The proteins of muscle – Actin

- Thin filaments are made of actin, troponin and tropomyosin
...

- Thin filaments are held in place by z lines, from one z lines to the next is a
sarcomere
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Notice = thick and thin filaments do not change in length
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Nerve impulse reaches an axon terminal and synaptic vesicles release acetylcholine
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ACh diffuses to the receptors on the sarcolemma and Na+ channels open , Na+
rushes into the cell
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A muscle AP spreads over the Sarcolemma and down transport tubules
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SR releases ca2+ into the sarcoplasm
5
...
= contraction cycle
begins
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The myosin head is activated when ATP binds to it and forms ADP + Pi
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It unbinds when ATP attaches again, the energy produced causes the myosin head to
return to the cocked position
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- Contraction occurs when calcium ions bind to troponin; this complex then pulls
tropomyosin away from the cross-bridge binding site
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- The calcium-troponin complex “pulls” tropomyosin off the myosin-binding site of
actin, thus allowing the binding of the cross-bridge
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Contraction cycle

- Repeating sequence of events that cause the thick & thin filaments to move past
each other
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Relaxation

- Acetylcholinesterase breaks down ACh within the synaptic cleft
- Muscle action potential ceases
- Ca2+ release channels close
- Active transport pumps Ca2+ back into storage in the sarcoplasmic reticulum
- Calcium-binding protein helps hold Ca2+ in SR
- Tropomyosin-troponin complex recovers binding site on the actin

Autonomic nervous system
- Innervates everything else (mainly smooth muscle)
- Sometimes described as the ‘involuntary’ nervous system
- Regulates function of internal organs
- motor pathways from brain to organs – blood vessels – heart – gut
- activators are stress, hyperglycemia, cold, exercise


Sympathetic responses:
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caused by physical or emotional stress -- “E situations” – emergency,
embarrassment, excitement, exercise
Alarm reaction = flight or fight response = dilation of pupils
this causes an increase of heart rate = decrease in blood flow to nonessential organs
increase in blood flow to skeletal & cardiac muscle – airways dilate & respiratory
rate increases = blood glucose level increase

Parasympathetic Responses
- Enhance “rest-and-digest” activities
- Mechanisms that help conserve and restore body energy during times of rest
- Normally dominate over sympathetic impulses
- Increases salivation, lacrimation, urination, digestion & defecation (SLUDD) and
decreased Heart Rate, diameter of airways and diameter of pupil
- Paradoxical fear when there is no escape route or no way to win – causes massive
activation of parasympathetic division – loss of control over urination and defecation
Somatic nervous system
- Somatic motor neurons innervate skeletal muscle to produce conscious, voluntary
movements
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Automatic nervous system
- The autonomic motor neurons regulate activities by either increasing (exciting) or
decreasing (inhibiting) ongoing activities of cardiac muscle, smooth muscle, and
glands
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Somatic vs Automatic





Both have afferent neurons
All somatic motor pathways consist of a single motor neuron
Autonomic motor pathways consists of two motor neurons in series – The first
autonomic neuron motor has its cell body in the CNS and its myelinated axon
extends to an autonomic ganglion
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Please learn the picture below, the purpose of this is that the same neurotransmitter can be
used for different purposes throughout the nervous system often they act on different receptor
subtypes

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